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Human Molecular Genetics Advance Access originally published online on April 30, 2007
Human Molecular Genetics 2007 16(13):1541-1556; doi:10.1093/hmg/ddm103
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

p27Kip1 localization depends on the tumor suppressor protein tuberin

Margit Rosner1, Angelika Freilinger1, Michaela Hanneder1, Naoya Fujita3, Gert Lubec2, Takashi Tsuruo3 and Markus Hengstschläger1,*

1 Medical Genetics, Obstetrics and Gynecology and 2 Department of Pediatrics, Medical University of Vienna, Währinger Gürtel 18–20, 1090 Vienna, Austria and 3 Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032, Japan

* To whom correspondence should be addressed. Tel: +43 1404007847; Fax: +43 1404007848; Email: markus.hengstschlaeger{at}meduniwien.ac.at

Received February 2, 2007; Accepted April 12, 2007

p27Kip1 plays an important role in cell cycle regulation by inhibiting cyclin–CDK complex activity in the nucleus. p27Kip1 is regulated by its concentration as well as by its subcellular localization. Tuberin, encoded by the tuberous sclerosis tumor suppressor gene TSC2, is a potent negative cell cycle regulator. We show herein, that tuberin induces nuclear p27 localization by inhibiting its 14-3-3-mediated cytoplasmic retention. Tuberin interferes with 14-3-3's counteracting effects on p27-mediated cell cycle arrest. Akt-mediated phosphorylation of p27, but not of tuberin, negatively regulates tuberin's potential to trigger p27 nuclear localization. In G0 cells, tuberin binds p27 triggering downregulation of p27's binding to 14-3-3 and of its cytoplasmic retention. At transition to S phase p27 is phosphorylated by Akt, tuberin/p27 complex levels are downregulated and binding of p27 to 14-3-3 increases triggering cytoplasmic retention of p27. These findings demonstrate p27 localization during the mammalian cell cycle to be under the control of the tumor suppressor tuberin.


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